They Are What You Eat: Can Nutritional Factors during Gestation and Early Infancy Modulate the Neonatal Immune Response?

The ontogeny of the human immune system is sensitive to nutrition even in the very early embryo, with both deficiency and excess of macro- and micronutrients being potentially detrimental. Neonates are particularly vulnerable to infectious disease due to the immaturity of the immune system and modulation of nutritional immunity may play a role in this sensitivity. This review examines whether nutrition around the time of conception, throughout pregnancy, and in early neonatal life may impact on the developing infant immune system

Regeneration of T-cell helper function in zinc-deficient adult mice

Diets deficient in zinc cause rapid atrophy of the thymus and loss of T-cell helper function in the young adult A/J mouse. Because zinc deficiency, as well as other nutritional deficiences, causes extensive damage to the immune system, the question arose as to whether zinc-deficient mice could repair the thymus and fully regenerate T-cell helper function if returned to diets containing adequate amounts of zinc. Five-week-old A/J female mice were fed either a zinc-deficient (<1 μg of Zn per g) or a zinc-adequate (50 μg of Zn per g) diet for 31 days. Histological examination of thymuses from the zinc-deficient mice revealed that the cortex was preferentially involuted and the thymus was about one-third of normal size. The direct plaque-forming cells produced per mouse spleen in response to immunization with sheep erythrocytes was 34% of normal; indirect plaque-forming cells were 18% of normal (Jerne plaque assay). After the deficient mice had been fed a zinc-adequate diet for 1 week, their response was nearly normal, except that the indirect response was 68% of controls; in this same period, the thymuses of these mice had quadrupled in size and exhibited a greatly enlarged cortex repopulated with immature thymocytes. By 2 weeks, the thymuses of the previously zinc-deficient mice were normal in size and appearance; however, there was a slight increases in numbers of indirect plaque-forming cells. By 4 weeks, the thymus weights, direct and indirect plaque-forming cell counts, and secondary response of the previously deficient mice were normal. Mice that were nearly athymic after 45 days of dietary zinc deficiency were also able to fully reconstruct the thymus and regenerate T-cell helper function. The data show that the zinc-deficient young adult mouse has the capacity to fully restore the T-cell-dependent antibody-mediated responses upon nutritional repletion